peptic ulcer disease

Assistant Professor
Ahmed Almerzoug
peptic ulcer disease (PUD)
• A (PUD) is a well-defined break in the GI mucosa (at
least 0.5 mm in diameter) that results from chronic acid
or pepsin secretions and the destructive effects of and
host response to Helicobacter pylori.]
• The first portion of the duodenum is the location of most
ulcers in Western populations, whereas gastric ulcers are
more frequent in Asia. PUD usually is chronic and focal
in distribution; only about 10% of patients have multiple
ulcers.
 Epidemiology
• About two thirds of persons with ulcers are men,
• the peak prevalence of peptic ulceration occurs in older adults.
• First-degree relatives have a threefold greater risk
• smokers and heavy drinkers of alcohol are more prone
• An association with blood type O also is recognized.
• (NSAIDs), including aspirin, for longer than 1 month.
Etiology

The balance between aggressive factors destructive to the GI

mucosa and defensive is disrupted.
• The primary aggressive factor is H. pylori. more than 80% of
duodenal and gastric ulcers
• The use of NSAIDS is the second most common cause of PUD.
• Other risk factors: advanced age, psychological and physical
stress, acid hypersecretion, cigarette smoking, use of certain
drugs.
H. pylori
• H. pylori can persist in the stomach indefinitely, and
infection with the bacterium remains clinically silent in
most affected persons.
• Approximately 20% of infected persons go on to
develop PUD, suggesting that other physiologic and
psychological (stress) factors are required for the
presentation of this disease.
NSAIDs
• NSAIDs is an etiologic factor in about 15% of cases of peptic ulcer.
• These drugs directly damage mucosa, reduce mucosal prostaglandin
production, and inhibit mucus secretion.
• Ulcers caused by NSAIDs are located more often in the stomach than in
the duodenum.
• The risk with NSAID use increases with age older than 60 years
• high-dosage long-term therapy;
• use of NSAIDs with long plasma half-lives (e.g., piroxicam) rather than
those with short half-lives (i.e., ibuprofen)
• concomitant use of alcohol, corticosteroids, anticoagulants
Other drugs
• The use of orally administered bisphosphonate drugs
(alendronate) for the treatment of osteoporosis is
associated with the development of esophageal and
gastric ulcers.
• H. pylori-negative, non-NSAID ulcer disease accounts
for about 10% of cases and occurs more often in older
adults.
Pathophysiology
• The secretion of acid and pepsin is controlled by two mechanisms: nervous and
hormonal.
• The vagus nerves are responsible for nervous control, and the hormone gastrin
is responsible for hormonal control.
• food stimulates gastrin release, gastrin stimulates parietal cells secrete
hydrochloric acid.
• caffeine, and histamine also are stimulants of parietal cell secretion of
hydrochloric acid.
• Physical and emotional stress, obsessive-compulsive behavior, parasitic
infections, high-dose corticosteroids enhance hypersecretion of stomach acid
Pathophysiology ……cont

• Alcohol and NSAIDs are directly injurious to the gastric mucosa

• Tobacco smoke can affect gastric mucosa by reducing levels of nitric
oxide, which is important for stimulating mucus secretion and
maintaining mucosal blood flow
• H. pylori cause inflammation of the gastric mucosa by producing
proteases and increasing gastrin release, which leads to increased
gastric acid production, acute gastritis, and eventually ulcer formation.
 Complications

• Ulcers can perforate into the peritoneal cavity (escape of stomach

contents) causing peritonitis. Arteries or veins in the muscular layer
may be eroded by ulcers (bleeding ulcer), giving rise to acute
hemorrhage, anemia, and potential shock.
• Untreated ulcers often heal by fibrosis, which can lead to pyloric
stenosis or gastric outlet obstruction. Complications are more common
in older adults and those with comorbid liver, kidney, and malignant
diseases.
• H. pylori are associated with the development of a low-grade gastric
mucosa-associated lymphoid tissue (MALT) lymphoma. Accordingly,
H. pylori has been classified as human carcinogen.
 Signs and Symptoms
• epigastric "burning pain that is long-standing (several
hours), sharply localized, and recurrent
• The discomfort of a duodenal ulcer manifests most
commonly on an empty stomach and frequently awakens
the patient in the middle of the night. Ingestion of food,
milk, or antacids provides rapid relief in most cases.
 Signs and Symptoms……cont
• patients with gastric ulcers, eating may precipitate
abdominal pain and Epigastric tenderness
• Changes in the character of pain may indicate the
development of complications. For example, increased
discomfort, loss of antacid relief, or pain radiating to the
back may signal deeper penetration or perforation
Signs and Symptoms……cont
Protracted vomiting a few hours after a
meal is a sign of gastric outlet (pyloric)
obstruction. Melena (bloody stools) or
black tarry stools indicate blood loss due
to GI hemorrhage.
Laboratory and Diagnostic Findings

• A peptic ulcer is diagnosed primarily by

fiberoptic endoscopic biopsy and laboratory
testing for H. pylori. During endoscopy, a biopsy
of the marginal mucosa adjacent to the ulcer is
performed to confirm the diagnosis and rule out
malignancy. A low red blood count may occur in
persons with a GI bleed.
 Medical Management

• In all patients who undergo peptic ulcer therapy, ulcerogenic factors

(e.g., smoking ,alcohol, NSAIDs, and corticosteroids; consumption
of foods that aggravate symptoms and stimulate gastric acid
secretion; persistent stress) should be eliminated
• proton pump inhibitor (PPI), is administered for 10 to 14 days;
treatment is extended for four or more weeks if complications occur.
If the patient is infected with H. pylori, inhibitors of gastric acid
secretion and at least two antimicrobial agents are recommended.
• omeprazole + clarithromycin (or metronidazole) and amoxicillin.for

2-3 wk
surgery
• Today, surgery is reserved primarily for complications of PUD
such as significant bleeding (when unresponsive to coagulant
endoscopic procedures), perforation, and gastric outlet
obstruction.
• In the surgical treatment of chronic gastric and duodenal ulcers,
attempts are made to reduce the amount of acid secretion by
sectioning the vagus nerves (vagotomy) and by removing the
gastrin-bearing area of the mucosa, the antrum (partial
gastrectomy).
 Oral Complications and Manifestations
• H. pylori is found in dental plaque and may serve as a reservoir of
infection and reinfection along the alimentary tract. Good oral hygiene
measures and periodic scaling and prophylaxis may be useful in
reducing the spread of this organism.
• The use of systemic antibiotics for PUD may result in fungal
overgrowth (candidiasis) or median rhomboid glossitis in the oral
cavity. A course of antifungal agents should be prescribed to resolve
the fungal infection.
• The erosion of the enamel is the less common oral manifestation of
PUD. Enamel erosion is the result of persistent regurgitation of gastric
juices into the mouth when pyloric stenosis occurs.
 Oral effects of medications
• Medications taken by patients for the treatment of PUD can produce ora
manifestations.
• PPIs can alter taste perception.
• Cimetidine and ranitidine may have a toxic effect on bone marrow; anemia
agranulocytosis, or thrombocytopenia.
• Mucosal ulcerations may be a sign of agranulocytosis, anemia may
manifest as mucosal pallor, and thrombocytopenia as gingival bleeding o
petechiae
• Xerostomia has been associated with the use of anticholinergic drugs.
 Dental Management and Recommendations

• The dentist must identify intestinal symptoms through

careful history includes a careful review of medications
• If GI symptoms are suggestive of active disease, a medical
referral is needed.
• When the patient is under control, the dentist should follow
physician guidelines.
Risk Assessment
Severe disease or poor control is evident by:
• 1. Ongoing pain.
• 2. Blood in the stool.
• 3. Anemia.
• 4. Recent physician visits.
• 5. Hospitalization in which medical treatment has not
relieved the condition.
Risk assessment
• Antibiotics: the selection of antibiotics for dental issues may need to be altered based on the antibiotics used
recently in the treatment of PUD.
• Bleeding: Bleeding from oral tissues is not an issue with PUD. In contrast, GI bleeding associated with PUD
can be of major concern and lead to significant complications that can delay dental treatment.
• Capacity to Tolerate Care: A patient with ongoing signs and symptoms of active PUD is not a candidate for
routine dental care.
 Drug Considerations
• The dentist should avoid prescribing aspirin and other NSAIDs because of the
irritative effects on the GI epithelium. Acetaminophen is recommended instead.
If NSAIDS are used, a COX-2-selective inhibitor (Celebrex) given in
combination with a PPI is advised for short-term use to reduce the risk of GI
bleeding. Analgesia should be the lowest dose for the shortest period to achieve
the desired effect.
• Acid-blocking drugs, such as cimetidine, decrease the metabolism of certain
dentally prescribed drugs (diazepam, lidocaine, tricyclic antidepressants) and
enhance the duration of action of these medications. Antacids also impair the
absorption of tetracycline, erythromycin, and oral iron, thereby preventing the
attainment of optimal blood levels of these drugs. To avoid this problem,
antibiotics and dietary supplements should be taken 2 hours before or 2 hours
after antacids are ingested.